Endothelial cell dysfunction is an early and ubiquitous feature of cardiovascular disease, which includes a loss of vasodilator capacity resulting in increased vascular reactivity. Vasodilator capacity is due to the synthesis of nitric oxide (NO) and the activation of endothelium-dependent hyperpolarization (EDH). In myogenically active cerebral arteries, mimicking dysfunction by loss of endothelial nitric oxide leads to intense vasospasm (Toda et al., 1991). In small resistance arteries and arterioles, vascular smooth muscle (VSM) contraction is predominately the result of Ca2+ influx through L-type voltage-gated calcium channels (VGCCs). These vessels provide the bulk of the peripheral vascular resistance, direct tissue blood flow and are targeted therapeutically by Ca2+ channel blockers, particularly the dihydropyridines (Nelson et al., 1990). VSM also contain T-type channels, which appear to provide a larger contribution to myogenic tone in small arteries, relative to L-type VGCCs, although remaining of secondary importance (Hansen, 2015). A role for T-type VGCCs may at first seem surprising, as the channels have a low activation threshold and inactivate rapidly. Consistent with this property, in cerebral arteries the functional contribution of T-type VGCCs relative to L-type appears greater at low intraluminal pressure, when the membrane potential is more hyperpolarized. However, in isolated cerebral artery VSM T-type window currents peak at around -40mV in the absence of L-type channels, and also contribute to the combined window currents when both forms are active, supporting a significant but modest role for these channels in myogenic tone (Harraz et al, 2014). The pore-forming α1subunits, CaV3.1 and 3.2 have been found in VSM, with CaV3.2 forming a microdomain with ryanodine receptors and large-conductance Ca-activated K channels in cerebral arteries, serving to attenuate vasoconstriction (Harraz et al, 2015). However, this may be a characteristic of cerebral arterioles, as similar microdomains do not appear operate in peripheral arterioles (Mullan et al., 2017). Membrane potential measurements in intact cerebral arteries revealed that block of NO synthesis was followed by the appearance of depolarizing spikes, apparently mediated by a de novoinvolvement of T-type VGCCs. These events modified myogenic tone giving rise to vasospasm (McNeish et al., 2010). The emergence of T-type VGCC in cerebrovascular VSM has also been demonstrated using patch-clamp recording in isolated cells and suggested to be mediated through cGMP/PKG signalling (Harraz et al., 2014). However, the overall effect of NO in cerebral arteries is complex, as it also inhibits L-type VGCCs and activates RyRs, the latter supressing vasoconstriction via BKCa (Yuill et al., 2010). Clinically, combined block of T- and L-type VGCCs appears to be more effective in treating hypertension than L-type block alone (Hansen, 2015), which at least in part may indicate an action against raised vascular reactivity. The possibility T-type channels underlie vasospasm in resistance arteries outside of the cerebral circulation has not been addressed, although it is known that T-type VGCCs are recruited in mouse resistance arteries once endothelial cell NO-signalling is compromised (Howitt et al., 2013). Other considerations include the extent to which an increase in T-type VGCC input might contribute to the vasoconstrictor response of non-myogenic arteries and possible interactions with endothelial signalling. In terms of vasoconstriction, a reduction while sustaining myogenic tone for autoregulation would be a desirable outcome. With the endothelium, bidirectional signalling involving VSM VGCCs can modulate endothelial cell microdomains, supressing vasoconstriction and possibly involving T-type VGCCs, (Garland et al., 2017). Discovering how and to what extent T-type VGCCs contribute to small artery vasospasm may therefore provide novel targets to treat cardiovascular disease.